Brunner syndrome

Brunner syndrome is caused by a monoamine oxidase A (MAOA) deficiency, which leads to an excess of monoamines in the brain, such as serotonin, dopamine, and norepinephrine (noradrenaline). In both mice and humans, a mutation was located on the eighth exon of the MAO-A gene, which created a dysfunctional MAO-A gene.[5][6] The regular function of MAO-A, breaking down monoamines, is disrupted, and monoamines build up within the brain. Mice that lacked a functional MAO-A gene displayed higher levels of aggression, in comparison to mice with a functional MAO-A gene.[6]

Progesterone & Rauwolfia Serpentina (containing Reserpine) are a possible treatment as they both increase MAO-A activity.

Brunner Syndrome was described in 1993 by H.G. Brunner and his colleagues upon the discovery of a particular genetic defect in male members of a large Dutch family.[5] Brunner found that all of the male family members with this defect reacted aggressively when angry, fearful, or frustrated. The defect discovered was later found to be a mutation in the gene that codes for monoamine oxidase A (MAOA gene).[5] Brunner said that an "MAO-A deficiency is associated with a recognizable behavioural phenotype that included disturbed regulation of impulsive aggression".[5]

A letter published by Hebebrand and Klug (1995)[7] criticized Brunner's findings for not using strict DSM criteria.

Brunner's findings have been used to argue that genetics, rather than decision-making processes, can cause criminal activity.[8] Evidence supporting the genetic defense stems from both Brunner's findings and a series of studies on mice.[9] To prove the correlation between MAO-A deficiency and aggression in courts, it is often contended that individuals cannot be held accountable for their genes, and as a result, should not be held responsible for their dispositions and resulting actions.[8][9]